Pathogenesis of Viral Hemorrhagic Fevers: Rift Valley Fever and Lassa Fever Contrasted
| العنوان: | Pathogenesis of Viral Hemorrhagic Fevers: Rift Valley Fever and Lassa Fever Contrasted |
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| المؤلفون: | C. J. Peters, John C. Morrill, George W. Anderson, Ching-Tong Liu, P. B. Jahrling |
| المصدر: | Clinical Infectious Diseases. 11:S743-S749 |
| بيانات النشر: | Oxford University Press (OUP), 1989. |
| سنة النشر: | 1989 |
| مصطلحات موضوعية: | Microbiology (medical), Arenavirus, Rift Valley Fever, biology, business.industry, viruses, medicine.disease, biology.organism_classification, Virology, Virus, Viral hemorrhagic fever, Hemorrhagic Fevers, Lassa Fever, Infectious Diseases, Phlebovirus, Immunology, medicine, Animals, Humans, Viral disease, Rift Valley fever, Lassa fever, business |
| الوصف: | Although many viral infections have on occasion been associated with hemorrhagic complications, infection with any of several RNA viruses regularly results in vascular involvement and the syndrome called viral hemorrhagic fever (VHF). In spite of clinically useful similarities among various VHFs, there are significant differences in their pathogenesis and clinical evolution; these are often related to characteristics of their viral taxon. Infection with Rift Valley fever (RVF) virus, a phlebovirus, appears to be regulated by interferon and terminated by neutralizing antibody. In contrast, Lassa fever (LF) virus, an arenavirus, is resistant to interferon, and LF is terminated by cellular immune effector mechanisms. The lytic virus-cell interaction typical of RVF virus suggests its major effects occur by direct, virus-induced cellular necrosis, particularly in the liver. In the primate RVF model, disseminated intravascular coagulation (DIC) may be important. LF virus--characteristically noncytopathic--may exert its effects through induction of mediator secretion from infected macrophages. DIC does not appear to be a central pathogenetic mechanism in LF. Pichinde virus, which is not pathogenic for humans, provides an alternate model for study of LF. Infected guinea pigs do not show histologic lesions that could explain their body wasting, cardiovascular deterioration, and pulmonary edema. In the heart, for example, loss of tissue mass, protein, and contractile function proceed without direct viral involvement or myocarditis. Sulfidopeptide leukotrienes have been implicated as one relevant soluble mediator participating in the disease state. |
| تدمد: | 1537-6591 1058-4838 |
| DOI: | 10.1093/clinids/11.supplement_4.s743 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3c5e146bdb947cfcb70c6176c23f625f https://doi.org/10.1093/clinids/11.supplement_4.s743 |
| رقم الانضمام: | edsair.doi.dedup.....3c5e146bdb947cfcb70c6176c23f625f |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15376591 10584838 |
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| DOI: | 10.1093/clinids/11.supplement_4.s743 |